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Depolarization of Mitochondria in Endothelial Cells Promotes Cerebral Artery Vasodilation by Activation of Nitric Oxide Synthase
Author(s) -
Prasad V. G. Katakam,
Edina A. Wappler-Guzzetta,
Paige S. Katz,
Ibolya Rutkai,
Ádám Institóris,
Ferenc Domoki,
Tamás Gáspár,
Samuel M. Grovenburg,
James A. Snipes,
David W. Busija
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300560
Subject(s) - nitric oxide , vasodilation , depolarization , nitric oxide synthase , mitochondrion , endothelial nitric oxide synthase , endothelium , chemistry , medicine , cardiology , microbiology and biotechnology , biology , biochemistry , enos
Mitochondrial depolarization after ATP-sensitive potassium channel activation has been shown to induce cerebral vasodilation by the generation of calcium sparks in smooth muscle. It is unclear, however, whether mitochondrial depolarization in endothelial cells is capable of promoting vasodilation by releasing vasoactive factors. Therefore, we studied the effect of endothelial mitochondrial depolarization by mitochondrial ATP-sensitive potassium channel activators, BMS-191095 (BMS) and diazoxide, on endothelium-dependent vasodilation.

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